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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2009;29:617.)
© 2009 American Heart Association, Inc.

Editorials

Kallikrein–Kinin System in Neovascularization

Michael Bader

From the Max Delbrück Center for Molecular Medicine (MDC), Berlin, Germany.

Correspondence to Michael Bader, PhD, Max-Delbrück-Center for Molecular Medicine (MDC), Robert-Rössle-Str. 10, D-13125 Berlin-Buch, Germany. E-mail mbader@mdc-berlin.de

An extract of the first 250 words of the full text is provided, because this article has no abstract.

The formation of new blood vessels is viewed completely differently by cardiologists than by oncologists and ophthalmologists. Whereas the former try to stimulate this process, the latter put all efforts into blocking it. In any case, factors involved in neovascularization are of highest therapeutic relevance. The article by Stone et al in this issue of ATVB¹ corroborates that the kallikrein–kinin system (KKS) is one very important but yet underestimated player in this process. This peptide hormone system acts via kinins which are generated from precursors, called kininogens, by enzymes called kallikreins, two of which exist, plasma (PK) and tissue kallikrein (TK). The most important kinin is the nonapeptide bradykinin, which activates the G protein–coupled receptor B2. When kininase I (carboxypeptidase M or N) truncates the peptide by 1 amino acid at the C terminus, the resulting des-Arg⁹bradykinin binds the B1 receptor. Interestingly, this receptor is 1 of the rare G protein–coupled receptors, which is inducible by inflammatory mediators, in contrast to the B2 receptor, which is constitutively expressed in multiple cell types.² Kininase II degrades kinins further to inactive fragments and is identical to angiotensin-converting enzyme (ACE). Consequently ACE inhibitors, one of the most popular classes of cardiovascular drugs, not only inhibit angiotensin generation but also stabilize kinins with important consequences in particular in their effects on vessel formation.

See accompanying article on page 657

The first evidence for a role of the KKS in neovascularization was published already more than 15 years ago. Hu and Fan³ showed that . . . [Full Text of this Article]

Related Article:

Critical Role of Tissue Kallikrein in Vessel Formation and Maturation: Implications for Therapeutic Revascularization

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Arterioscler Thromb Vasc Biol 2009 29: 657-664. [Abstract] [Full Text] [PDF]